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We also tested the ability of DEAQ to inhibit pathogenicity of Junin and Chikungunya viruses and observed that DEAQ inhibits those two viruses with EC50’s similar to those of AQ (Supplementary Table 2). Other pathogenic agents, including cholera toxin 37 , Pseudomonas aeruginosa exotoxin A 38 , Poliovirus 3 18 and Herpes simplex virus 1 39 are transported in a retrograde fashion to the endoplasmic reticulum (ER) and retrotranslocated into the cytoplasm by the host ER-associated degradation pathway 37,38. We observed that cytotoxicity mediated by those pathogens was not blocked by AQ (Table 3 and Supplementary Fig, super-steroid.com reviews. In addition, the inability of AQ to inhibit cholera and Pseudomonas toxins, which are both ADP-rybosyltransferases, suggests that AQ’s adverse effect on diphtheria toxin (Fig. Another group of pathogens enter the cytoplasm by ways that do not rely on the acidification of endosomes and include Human Cytomegalovirus 40 and Respiratory syncytial virus 41. We determined that AQ did not reduce the pathogenicity of those viruses (Table 3). This data supports the conclusion that AQ inhibits the entry of toxins into the cytoplasm from acidified endosomes. The discovery and development of novel drugs against biological threat agents such as Bacillus anthracis and Ebola virus, is an important concern worldwide. We have shown that AQ is a broad-spectrum drug that could be applied rapidly to cure biological emergencies caused by the several identified pathogens (Fig. For example, the current Ebola crisis has already killed more than 10,000 people in 2014 and 2015. Repurposing of a compound with well-established safety and pharmacokinetic profiles’as well as proven high-volume GMP manufacturing’may be the only way that a therapy can be tested and deployed in time to protect the 21 + million people in the three hardest-hit West African countries. Mechanism of action of Amodiaquine. AQ reduces the activities of pathogens that enter into host cytoplasm from acidified endosomes by exploiting cellular cathepsin B. AQ does not inhibit the entry of pathogens that enter through a retrograde fashion to the endoplasmic reticulum (ER) and retrotranslocated into the cytoplasm by the host ER-associated degradation pathway or by pH-independent entry into cytoplasm. To help address this Ebola crisis, as we were preparing this manuscript, we communicated our discoveries to Medecins Sans Frontieres (MSF, Doctors Without Borders) and encouraged them to explore whether the administration of AQ in West African countries hit by Ebola epidemic is associated with a reduced mortality due to Ebola infections. MSF conducted a study and observed that the administration of AQ provided a substantial protection against Ebola mortality and reduced the mortality risk by 31% and in this study MSF acknowledged the authors of this study (https://www. As seen in current Ebola epidemic, the human host can be co-exposed to numerous deadly pathogens and thus the infected individual will need to take numerous countermeasures (each with their own side-effects) to protect against multiple infectious organisms. Therefore, therapies capable of inhibiting multiple pathogens are needed. Broad-spectrum anti-pathogen drugs, capable of simultaneously inhibiting numerous unrelated pathogens, could be developed by targeting host proteins commonly exploited by those pathogens. In this work we show that AQ inhibits the host target rather than the pathogen, which makes AQ host-oriented broad-spectrum antimicrobial that is less likely to be circumvented by pathogen mutations that lead to microbial resistance to the countermeasure. AQ was discovered by Parke-Davis in the 1940s and was approved by the FDA as an anti-malarial in the late 1940s and early 1950s under the trade name Camoquine. AQ is currently on the WHO’s Model List of Essential Medicines. Today AQ is recommended as a frontline anti-malarial therapy in combination with artemisinin. AQ belongs to the ‘quinoline antimalarials’ (Reviewed in 42 ). AQ inhibits Plasmodium falciparum phosphoethanolamine methyltransferase, an enzyme found in malarial parasites but not in humans 43.
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